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ES-E14

RRID:CVCL_C320

Organism

Mus musculus

Comments

Part of: ENCODE project mouse cell lines. Omics: DNA methylation analysis. Omics: Genome sequenced. Omics: H3K27ac ChIP-seq epigenome analysis. Omics: H3K27me3 ChIP-seq epigenome analysis. Omics: H3K36me3 ChIP-seq epigenome analysis. Omics: H3K4me1 ChIP-seq epigenome analysis. Omics: H3K4me3 ChIP-seq epigenome analysis. Omics: H3K9ac ChIP-seq epigenome analysis. Omics: H3K9me2 ChIP-seq epigenome analysis. Omics: H3K9me3 ChIP-seq epigenome analysis. Omics: Transcriptome analysis. Breed/subspecies: 129P2/Ola. DT Created: 22-10-12; Last updated: 07-09-18; Version: 14

Proper Citation

RRID:CVCL_C320

Category

Embryonic stem cell DT Created: 22-10-12; Last updated: 07-09-18; Version: 14

Sex

DT Created: 22-10-12; Last updated: 07-09-18; Version: 14

Synonyms

E14, E-14, ES (E14) DT Created: 22-10-12, Last updated: 07-09-18, Version: 14

Cross References

BTO; BTO:0005136 EFO; EFO_0007075 4DN; 4DNSRR6CIPYP BioSamples; SAMEA2155660 ENCODE; ENCBS033ENC ENCODE; ENCBS042ENC ENCODE; ENCBS043ENC ENCODE; ENCBS054SMP ENCODE; ENCBS324NLT GEO; GSM344759 GEO; GSM344760 GEO; GSM397410 GEO; GSM397411 GEO; GSM413111 GEO; GSM413112 GEO; GSM413113 GEO; GSM413117 GEO; GSM413118 GEO; GSM413119 GEO; GSM413123 GEO; GSM413124 GEO; GSM413125 GEO; GSM413129 GEO; GSM413130 GEO; GSM413131 GEO; GSM413135 GEO; GSM413136 GEO; GSM413137 GEO; GSM413141 GEO; GSM413142 GEO; GSM413143 GEO; GSM413147 GEO; GSM413148 GEO; GSM413149 GEO; GSM413153 GEO; GSM413154 GEO; GSM413155 GEO; GSM1000121 GEO; GSM1000123 GEO; GSM1000124 GEO; GSM1000125 GEO; GSM1000126 GEO; GSM1003750 GEO; GSM1003751 GEO; GSM1003756 GEO; GSM1003799 GEO; GSM1003807 GEO; GSM1003809 GEO; GSM1003810 GEO; GSM1014154 Wikidata; Q54832448 DT Created: 22-10-12; Last updated: 07-09-18; Version: 14

Hierarchy

DT Created: 22-10-12; Last updated: 07-09-18; Version: 14

Originate from Same Individual

DT Created: 22-10-12; Last updated: 07-09-18; Version: 14

Micropattern differentiation of mouse pluripotent stem cells recapitulates embryo regionalized cell fate patterning.

  • Morgani SM
  • Elife
  • 2018 Feb 7

Literature context:


Abstract:

During gastrulation epiblast cells exit pluripotency as they specify and spatially arrange the three germ layers of the embryo. Similarly, human pluripotent stem cells (PSCs) undergo spatially organized fate specification on micropatterned surfaces. Since in vivo validation is not possible for the human, we developed a mouse PSC micropattern system and, with direct comparisons to mouse embryos, reveal the robust specification of distinct regional identities. BMP, WNT, ACTIVIN and FGF directed mouse epiblast-like cells to undergo an epithelial-to-mesenchymal transition and radially pattern posterior mesoderm fates. Conversely, WNT, ACTIVIN and FGF patterned anterior identities, including definitive endoderm. By contrast, epiblast stem cells, a developmentally advanced state, only specified anterior identities, but without patterning. The mouse micropattern system offers a robust scalable method to generate regionalized cell types present in vivo, resolve how signals promote distinct identities and generate patterns, and compare mechanisms operating in vivo and in vitro and across species.

Funding information:
  • Cancer Research UK - 06-914/915(United Kingdom)
  • Eunice Kennedy Shriver National Institute of Child Health and Human Development - R01HD080699()
  • National Cancer Institute - P30CA008748()
  • National Institute of Diabetes and Digestive and Kidney Diseases - R01DK084391()
  • National Science Foundation - PHY1502151()
  • NYSTEM - C029568()

Mapping the Mouse Cell Atlas by Microwell-Seq.

  • Han X
  • Cell
  • 2018 Feb 22

Literature context:


Abstract:

Single-cell RNA sequencing (scRNA-seq) technologies are poised to reshape the current cell-type classification system. However, a transcriptome-based single-cell atlas has not been achieved for complex mammalian systems. Here, we developed Microwell-seq, a high-throughput and low-cost scRNA-seq platform using simple, inexpensive devices. Using Microwell-seq, we analyzed more than 400,000 single cells covering all of the major mouse organs and constructed a basic scheme for a mouse cell atlas (MCA). We reveal a single-cell hierarchy for many tissues that have not been well characterized previously. We built a web-based "single-cell MCA analysis" pipeline that accurately defines cell types based on single-cell digital expression. Our study demonstrates the wide applicability of the Microwell-seq technology and MCA resource.

Funding information:
  • NIAID NIH HHS - AI047380(United States)

Engineered Multivalent Sensors to Detect Coexisting Histone Modifications in Living Stem Cells.

  • Delachat AM
  • Cell Chem Biol
  • 2018 Jan 18

Literature context:


Abstract:

The regulation of fundamental processes such as gene expression or cell differentiation involves chromatin states, demarcated by combinatorial histone post-translational modification (PTM) patterns. The subnuclear organization and dynamics of chromatin states is not well understood, as tools for their detection and modulation in live cells are lacking. Here, we report the development of genetically encoded chromatin-sensing multivalent probes, cMAPs, selective for bivalent chromatin, a PTM pattern associated with pluripotency in embryonic stem cells (ESCs). cMAPs were engineered from a set of PTM-binding (reader) proteins and optimized using synthetic nucleosomes carrying defined PTMs. Applied in live ESCs, cMAPs formed discrete subnuclear foci, revealing the organization of bivalent chromatin into local clusters. Moreover, cMAPs enabled direct monitoring of the loss of bivalency upon treatment with small-molecule epigenetic modulators. cMAPs thus provide a versatile platform to monitor chromatin state dynamics in live cells.

Funding information:
  • PHS HHS - P60-05130(United States)

A Chemical-Genetic Approach Reveals the Distinct Roles of GSK3α and GSK3β in Regulating Embryonic Stem Cell Fate.

  • Chen X
  • Dev. Cell
  • 2017 Dec 4

Literature context:


Abstract:

Glycogen synthase kinase 3 (GSK3) plays a central role in diverse cellular processes. GSK3 has two mammalian isozymes, GSK3α and GSK3β, whose functions remain ill-defined because of a lack of inhibitors that can distinguish between the two highly homologous isozymes. Here, we show that GSK3α and GSK3β can be selectively inhibited in mouse embryonic stem cells (ESCs) using a chemical-genetic approach. Selective inhibition of GSK3β is sufficient to maintain mouse ESC self-renewal, whereas GSK3α inhibition promotes mouse ESC differentiation toward neural lineages. Genome-wide transcriptional analysis reveals that GSK3α and GSK3β have distinct sets of downstream targets. Furthermore, selective inhibition of individual GSK3 isozymes yields distinct phenotypes from gene deletion, highlighting the power of the chemical-genetic approach in dissecting kinase catalytic functions from the protein's scaffolding functions. Our study opens new avenues for defining GSK3 isozyme-specific functions in various cellular processes.

Funding information:
  • NICHD NIH HHS - T32 HD060549()
  • NINDS NIH HHS - R01 NS048276(United States)

A lncRNA fine tunes the dynamics of a cell state transition involving Lin28, let-7 and de novo DNA methylation.

  • Li MA
  • Elife
  • 2017 Aug 18

Literature context:


Abstract:

Execution of pluripotency requires progression from the naïve status represented by mouse embryonic stem cells (ESCs) to a state capacitated for lineage specification. This transition is coordinated at multiple levels. Non-coding RNAs may contribute to this regulatory orchestra. We identified a rodent-specific long non-coding RNA (lncRNA) linc1281, hereafter Ephemeron (Eprn), that modulates the dynamics of exit from naïve pluripotency. Eprn deletion delays the extinction of ESC identity, an effect associated with perduring Nanog expression. In the absence of Eprn, Lin28a expression is reduced which results in persistence of let-7 microRNAs, and the up-regulation of de novo methyltransferases Dnmt3a/b is delayed. Dnmt3a/b deletion retards ES cell transition, correlating with delayed Nanog promoter methylation and phenocopying loss of Eprn or Lin28a. The connection from lncRNA to miRNA and DNA methylation facilitates the acute extinction of naïve pluripotency, a pre-requisite for rapid progression from preimplantation epiblast to gastrulation in rodents. Eprn illustrates how lncRNAs may introduce species-specific network modulations.

Funding information:
  • NCI NIH HHS - R01 CA139067()
  • NCI NIH HHS - R21 CA175560()
  • Wellcome Trust - P01 CA013106()

DNA methylation directs genomic localization of Mbd2 and Mbd3 in embryonic stem cells.

  • Hainer SJ
  • Elife
  • 2016 Nov 16

Literature context:


Abstract:

Cytosine methylation is an epigenetic and regulatory mark that functions in part through recruitment of chromatin remodeling complexes containing methyl-CpG binding domain (MBD) proteins. Two MBD proteins, Mbd2 and Mbd3, were previously shown to bind methylated or hydroxymethylated DNA, respectively; however, both of these findings have been disputed. Here, we investigated this controversy using experimental approaches and re-analysis of published data and find no evidence for methylation-independent functions of Mbd2 or Mbd3. We show that chromatin localization of Mbd2 and Mbd3 is highly overlapping and, unexpectedly, we find Mbd2 and Mbd3 are interdependent for chromatin association. Further investigation reveals that both proteins are required for normal levels of cytosine methylation and hydroxymethylation in murine embryonic stem cells. Furthermore, Mbd2 and Mbd3 regulate overlapping sets of genes that are also regulated by DNA methylation/hydroxymethylation factors. These findings reveal an interdependent regulatory mechanism mediated by the DNA methylation machinery and its readers.